Term
| what tissues usually have more cholesterol |
|
Definition
| liver, intestine, steroid tissue |
|
|
Term
| what tissues are sterodic |
|
Definition
| adrenal cortex, testes, ovaries |
|
|
Term
| what is the liver's role in cholesterol metabolism |
|
Definition
| synthesis, recieves it from chylomicrons, can derive it from HDL, distributes it in LDL |
|
|
Term
|
Definition
|
|
Term
| what can increased levels of cholesterol cause |
|
Definition
|
|
Term
| what are the functions of cholesterol |
|
Definition
| membrane components providing ridigity, precursor of bile salts, steroids, and vitamin D |
|
|
Term
| what is a steroid nucleus composed of |
|
Definition
|
|
Term
| why is cholesterol hydrophobic |
|
Definition
| lots of C/H and little O/N |
|
|
Term
| how can you make a cholesterol less soluble, why does this happen |
|
Definition
| esterification adds some C/H but lots of O increasing solubility |
|
|
Term
| how can you make cholesterol more soluble, give an example of a substance |
|
Definition
| add O/N like in bile salts |
|
|
Term
| where is cholesterol made |
|
Definition
|
|
Term
| HMG CoA Synthase is used in cholesterol synthesis and what other process |
|
Definition
|
|
Term
| HMG CoA Synthase is used in cholesterol synthesis and ketone breakdown, how does that work out when these functions are metabolically opposite |
|
Definition
| the enzyme is in different places in the cell allowing it to be regulated differently |
|
|
Term
| what influences synthesis of cholesterol |
|
Definition
| a well fed state where there is lots of energy and carbon skeletones available or when cholesterol is low |
|
|
Term
| what is the carbon skeleton used to make cholesterol |
|
Definition
|
|
Term
| what is the first reaction in cholesterol synthesis |
|
Definition
| 2 acetyl CoA --> acetoacetyl CoA |
|
|
Term
| after making acetoacetyl CoA, what happens next in cholesterol synthesis. what substrates and enzymes are needed |
|
Definition
| acetoacetyl CoA + acetyl CoA --> HMG-CoA. using HMG CoA synthase |
|
|
Term
| aftr making HMG-CoA in cholesterol synthesis, what happens next, what substrates and enzymes are needed |
|
Definition
| HMG-CoA + NADPH --> NADP + mevalonate. using HMG-CoA reductase |
|
|
Term
| what is the rate limiting and comitting enzyme in cholesterol sytnesis |
|
Definition
|
|
Term
| what enzyme is targeted by statin drugs |
|
Definition
|
|
Term
| after mevalonate is made in cholesterol synthesis, what happens next |
|
Definition
| mevalonate is added and the molecule cyclicizes. |
|
|
Term
| what is required to do cholesterol synthesis |
|
Definition
| 16 acetyl CoA, 6 mevalonate, ATP, NADH |
|
|
Term
| how do we reverse cholesterol synthesis |
|
Definition
| you dont, most of the enzymes are irreversible |
|
|
Term
| how does cholesterol synthesis work when the intermediates need to be soluble in the cytoplasm |
|
Definition
| they are charged until squalene formation which is associated with a carrier protein that makes it work out |
|
|
Term
| what is defective in smith lemi optiz syndrome |
|
Definition
| enzyme of conversion of lanosterol to cholesterol |
|
|
Term
| what type of inheritence is smith lemi optiz syndrome |
|
Definition
|
|
Term
| what are the symptoms of smith lemi optiz symdrome |
|
Definition
| mental retardation, ambygous genitalis, hypotonia, microencephalphy, syndactyly, limb abnormalities, deformatities, polydactyl |
|
|
Term
| what are the different ways you can increase HMG CoA reductase activity |
|
Definition
| increase transceription, activate or inactivate covalently, influence the turnover or amount of degration |
|
|
Term
| what ocntrols transcription of HMG CoA reductase |
|
Definition
|
|
Term
| what happens to HMG CoA reductase when there is an increase in sterols |
|
Definition
| SCAP/SERBP complex biinds to sterol in the ER, stopping its transctiption |
|
|
Term
| what happens to HMG CoA reductase when there are low sterols |
|
Definition
| SCAP/SERBP complex goes to the golgi and releases SERBP, SERBP finds the SRE (enhancer) and turns on transcription of HMG CoA reductase |
|
|
Term
| what is another way, other than SERBP/SCAP, that transcription of HMG CoA reductase can be accomplished |
|
Definition
|
|
Term
| in what covalently modified state is HMG CoA reductase active |
|
Definition
|
|
Term
| what can cause phosphorlyation of HMG CoA reductase |
|
Definition
|
|
Term
| what can cause depohsophorlyation of HMG CoA reductase |
|
Definition
|
|
Term
| what affects turnover of HMG CoA reductase |
|
Definition
| elevated sterol causes HMG CoA reductase to be ubiquinated and degraded by preteasomes |
|
|
Term
|
Definition
| side group resembeles HMG CoA and competes competitivly for the HMG CoA reductase active site |
|
|
Term
| what is in the membrane of a micelle |
|
Definition
| phospholipids, cholesterol for rigidity, apo proteins |
|
|
Term
|
Definition
| esterified cholesterol, TAG |
|
|
Term
| what are the types of lipoproteins |
|
Definition
| chylomicrons, VLDL, LDL, HDL, chylomicron remnents, VLDL remnents |
|
|
Term
| what does chylomicrons transport |
|
Definition
| dietary lipids and cholesterol |
|
|
Term
|
Definition
|
|
Term
|
Definition
| cholesterol away from the liver |
|
|
Term
|
Definition
| cholesterol to the liver and reserve apolipoproteins |
|
|
Term
| what is another name for a VLDL remnent |
|
Definition
|
|
Term
| what makes up a majority of the chilomicron, what is its size dependent on |
|
Definition
| lots of fat, meal ingested |
|
|
Term
| what is the least dense and largest lipoprotein |
|
Definition
|
|
Term
| what is similar to a chilumicron |
|
Definition
|
|
Term
| compare the size and composition of a chilomicron to a VLDL |
|
Definition
| VLDL is smaller and more desne |
|
|
Term
| what lipoprotein has the most cholesterol |
|
Definition
|
|
Term
| what lipoprotein has the most protein |
|
Definition
|
|
Term
| what lipoprotein has the secon dmost cholesterol |
|
Definition
|
|
Term
| why do you need to fast before a lipoprofile? |
|
Definition
| if you ate you will see lots of chylomicrons because it takes a while for them to be processed. sugar and protein are made into VLDL and it needs to be processed. you need to stabilize the levels to get a good reading |
|
|
Term
| what is the function of apo-b48 |
|
Definition
| scaffolding to contain lipids and fat soluble vitamins |
|
|
Term
| what are the fat soluble vitamins |
|
Definition
|
|
Term
| why is apo b48 called that |
|
Definition
| because it is 48% of an apo B 100, their n-terminus is the same |
|
|
Term
| how is an apo B100 turned into an apo b48 |
|
Definition
| post transcriptional modification leads to an early stop codon, it is similar to a nonsense mutation |
|
|
Term
| what happens when a chylomicron gets into the blood |
|
Definition
| it gets APO CII and APO E from HDL |
|
|
Term
| what is the function of apo C II |
|
Definition
| activate lipoprotein lipase to digest fats |
|
|
Term
| what is the function of apo E |
|
Definition
| ligand for apo E receptors on the liver that clear chylomicron from the blood |
|
|
Term
| after the action of apo CII and lipoprotein lipase what happens to the contents of a chilomicron |
|
Definition
| the TAG is transfered into the cell and the glycerol is taken to the liver |
|
|
Term
| after the chilomicron unloads, what happens to the remnent |
|
Definition
| the apo C II is sent back to the HDL, apo E goes to the apo E receptor on the liver and is endocytosed with the rest of the remnent |
|
|
Term
|
Definition
|
|
Term
|
Definition
| apo B100 scaffolding and a newly synthesized lipid |
|
|
Term
| what happens to VLDL when it first enters the blood |
|
Definition
| it gets apo C II and apo E from HDL |
|
|
Term
| how does VLDL unload to tissues |
|
Definition
| apo C II activates lipoprotein lipase to digest TAG so it can get into the tissue, glycerol goes to the liver |
|
|
Term
| what is left over after a VLDL unloads |
|
Definition
|
|
Term
| what is one fate for an IDL (the more simple one) |
|
Definition
| apo E causes it to be endocytosed by the liver |
|
|
Term
| what is the fate of IDL (the longer one) |
|
Definition
| LDL gives its TAG to a HDL and the HDL gives the LDL a cholesterol ester making the IDL now a LDL |
|
|
Term
|
Definition
| it still has apo B100 so it goes to the receptors for it that show up on cells low in choesterol (they make receptors when low), LDL is then endocytosed into the cell |
|
|
Term
| where is cholesterol stored |
|
Definition
| liver, sterogenic tissues (tissues with high cholesterol demand) |
|
|
Term
| how is cholesterol stored |
|
Definition
| esterified by ACAT (the inside the cell enzyme) |
|
|
Term
|
Definition
| acyl CoA cholesterol acyltransferase |
|
|
Term
| in general why is LDL bad |
|
Definition
| it can be eaten by macrophages and foam cells can be made which causes fatty streaks which leads to plaque and vessel blockage |
|
|
Term
| describe the process that creates an atherosclerotic plack |
|
Definition
1. LDL, oxidents, chemicals, or free radicals damage the vessel
2. macrophages respond and end up eating damaged LDL with their SRA receptor
3. macrophages become foam cells
4. foam cells make a fatty streak
5. foam cells stimulate for smooth muscle and collagen to migrate to the area
6. some smooth muscle will become foam cells too |
|
|
Term
| what incrases someones risk for an atherosclerotic plaque |
|
Definition
| more LDL, more in the blood means more time to be processed |
|
|
Term
|
Definition
| increased blood sugar, oxidative stress, chemicals in tobacco |
|
|
Term
| how does increased blood sugar affect LDL |
|
Definition
| non-specific glycosylation |
|
|
Term
| what types of oxidative stress effect LDL |
|
Definition
| infection, smoking, drugs |
|
|
Term
| what can smoking and diabetes lead to |
|
Definition
|
|
Term
| what can protect against antioxidents |
|
Definition
|
|
Term
| where does Apo A1 come from |
|
Definition
|
|
Term
|
Definition
| aquire phospholipids with the help of ABCA1 to make HDL |
|
|
Term
| once made, what is the first thing HDL does, why |
|
Definition
| picks up Apo CII and Apo E so it can be a resivour |
|
|
Term
| how does HDL get cholesterol |
|
Definition
| ABCA1 helps it pick it up from the tissues |
|
|
Term
| what happens to cholesterol once inside a HDL |
|
Definition
| Apo A1 activates LCAT (which is floating in the blood) and LCAT esterifies it |
|
|
Term
| what does an HDL with activated cholesterol do |
|
Definition
| go to the liver to drop it off |
|
|
Term
| how does HDL drop cholesterol off at the liver |
|
Definition
| SR-B1 allows transfer of the ester to the liver using CETP |
|
|
Term
|
Definition
| cholesterol ester transfer protein |
|
|
Term
| what is hte inheritence of tangier disease |
|
Definition
| very rare, autosomal recessive |
|
|
Term
| what is defective in tangier disease |
|
Definition
|
|
Term
| what are the symptoms of tangier disease |
|
Definition
| no HDL, cholesterol accumulation, neuropathy, enlarged liver and spleen, early cardiovascular disease and athlerosclerosis |
|
|
Term
| what type of inherirence is type 1 hyperlipoprotenemia |
|
Definition
|
|
Term
| what is defective in type 1 hyperlipoprotenemia |
|
Definition
| Apo CII or lipoprotein lipase |
|
|
Term
| what are the symptoms of type 1 hyperlipoprotenemia |
|
Definition
| elevated TAG / chylomicrons in the blood, xanthomas, pancreatitis |
|
|
Term
| what type of inheritence is type 2 hyperlipoprotenemia |
|
Definition
|
|
Term
| what is defective in type 2 hyperlipoprotenemia |
|
Definition
|
|
Term
| what are the symptoms of type 2 hyperlipoprotenemia |
|
Definition
| xanthomas, high LDL, athlerosclerosis, cardiovascular disease |
|
|
Term
| what type of inheritence is type 3 hyperlipoprotenemia |
|
Definition
|
|
Term
| what genes does one need to have type 3 hyperlipoprotenemia |
|
Definition
|
|
Term
| what is defective in type 3 hyperlipoprotenemia |
|
Definition
| Apo 3, remnents will stay in the blood |
|
|
Term
| what are the symptoms of type 3 hyperlipoprotenemia |
|
Definition
| xanthomas, cardiocascular disease |
|
|
Term
| what does Apo E have to do with alzheimer's disease |
|
Definition
| Apo E4 for some reason indicates higher risk for the disease, two copies of the gene even higher |
|
|
Term
| what is the only way cholesterol steroid nuclei can leave the body, normally what percent would this be |
|
Definition
| pooped out when made into bile salts and not reabsorbed, 5% of bile salts |
|
|
Term
| why is the only way to get rid of steroid nuclei by pooping bile salts out |
|
Definition
| because it cant be broken down int he body |
|
|
Term
| describe the composition of bile salts, what makes it different from cholesterol, what do these changes provide functionally |
|
Definition
| it has more oxygen, glycine or tauring are added increasing solubility, amphitatic to emulsify |
|
|
Term
| why is there free cholesterol in bile salts |
|
Definition
|
|
Term
| what happens to bile salts when they are done doing their job |
|
Definition
| they are recirculated to the liver and used again |
|
|
Term
| why are there bile salts and acids |
|
Definition
| because bacteria in the intestines modify them |
|
|
Term
| what do bile acid sequesterants do |
|
Definition
| reduce serum cholesterol by positivly binding to the bile salt preventing them from being reacsorbed so more cholester must be used to make bile, removing it from the blood, reducing serum LDL and cardiovascular risk |
|
|
Term
| what is an example of a natural bile acid sequesterant |
|
Definition
|
|
Term
| what are bile acid sequesterants combine with for maximum functionality |
|
Definition
|
|
Term
| what is another name for choleithiasis |
|
Definition
|
|
Term
|
Definition
| because there isnt enough bile salts or there is too much cholesterol due to inefficient recycling, liver dysfunction, etc |
|
|
Term
| what do gall stones do to cause problems |
|
Definition
| block bile ducts leading to pain and infection of the gall bladder and pancrease |
|
|
Term
| how are gall stones treated |
|
Definition
| remove gall bladder or bile acid suppliments will dissolve them |
|
|
Term
| What does HDL deliver cholesterol to, what does the tissue need to be a candidate |
|
Definition
| Liver or steroidogenic tissue that expresses SRBI protein (specific) |
|
|
Term
| What is the difference between SRA and SRBI? |
|
Definition
|
|
Term
| What is the characteristic symptom of tangler disease |
|
Definition
|
|
Term
| What is the characteristic symptom of type 1 hyperlipidemia |
|
Definition
| No cardiac disease risk increase because you need to form LDL and in type1 you dont |
|
|
